American Journal of Epidemiology Vol. 177, No.

8
© The Author 2013. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of DOI: 10.1093/aje/kws300
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March 6, 2013

Original Contribution

Occupational Noise Exposure and Incident Hypertension in Men: A Prospective

Cohort Study

Ta-Yuan Chang*, Bing-Fang Hwang, Chiu-Shong Liu, Ren-Yin Chen, Ven-Shing Wang,

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Bo-Ying Bao, and Jim-Shoung Lai
* Correspondence to Dr. Ta-Yuan Chang, China Medical University, 91 Hsueh-Shih Road, Taichung 40402, Taiwan, Republic of China
(e-mail: tychang@mail.cmu.edu.tw).

Initially submitted March 19, 2012; accepted for publication June 25, 2012.

The associations between occupational noise exposure and hypertension remain controversial because of the
differences in study designs, exposure assessments, and confounding controls. This prospective study investi-
gated the relationship between noise exposure and the 10-year risk of hypertension. A cohort of 578 male
workers in Taiwan was followed from 1998 to 2008. All subjects were divided into high-, intermediate-, and low-
exposure groups on the basis of noise exposure assessment. Cox regression models were used to estimate the
relative risks of hypertension after adjustment for potential confounders. During the 7,805 person-years of follow-
up, 141 hypertension cases were identified. Significant increases of 3.2 (95% confidence interval (CI): 0.2, 6.2)
mm Hg in systolic blood pressure and 2.5 (95% CI: 0.1, 4.8) mm Hg in diastolic blood pressure between the
baseline and follow-up measurements were observed in the high-exposure group. Participants exposed to ≥85
A-weighted decibels (dBA) had a 1.93-fold (95% CI: 1.15, 3.22) risk of hypertension compared with those
exposed to <80 dBA. There was a significant exposure-response pattern (P = 0.016) between the risk of hyper-
tension and the stratum of noise exposure. Prolonged exposure to noise levels ≥85 dBA may increase males’
systolic and diastolic blood pressure levels. This association may translate into a higher incidence of
hypertension.

blood pressure; hypertension; men; occupational noise; prospective studies

Abbreviations: CI, confidence interval; dBA, A-weighted decibel(s); DBP, diastolic blood pressure; RR, relative risk; SBP, sys-
tolic blood pressure; SD, standard deviation.

Chronic exposure to noise has been associated with car-
diovascular disease, including ischemic heart disease (1),
myocardial infarction (2–5), coronary heart disease (6, 7),
and stroke (8). This association may exist because noise
exposure activates the sympathetic and endocrine systems
to affect the humoral and metabolic states of the human
organism, producing the increase in blood pressure and the
changes in other biological risk factors (such as blood
lipids and glucose levels) that promote the development of
hypertension and cardiovascular diseases (9).
The existence of an association between noise exposure
in occupational settings and hypertension is still controver-
sial. Occupational noise exposure has been associated with
a sustained elevation of blood pressure or with a higher
risk of hypertension in 2 retrospective cohort studies (10, 11),
2 repeated-measure studies (12, 13), and 9 cross-sectional
studies (14–22). However, the results of other studies are
inconsistent with these findings (23–31). Reasons for this
inconsistency may include differences in study design, dif-
ferences in exposure assessment, different degrees of
ability to control for potential confounders, and various
degrees of the use of hearing-protective devices at work.
One cohort study reported a relationship between occu-
pational noise exposure and the incidence of hypertension
(10). However, these results were limited by an exposure
bias caused by no adjustments for the use of hearing-
protective devices, and the association between noise expo-
sure and blood pressure was not reported. In addition,

818 Am J Epidemiol. 2013;177(8):818–825


important risk factors for hypertension, such as body mass
index, cigarette use, alcohol intake, regular exercise, salt
intake, and a family history of hypertension (32, 33), were
not considered. The objective of this study was to investi-
gate the relationship between prolonged exposure to occu-
pational noise and the 10-year incidence of hypertension
by taking these important factors into account.
MATERIALS AND METHODS
Study population
This study was conducted by performing a follow-up
study to a cross-sectional survey in an aircraft manufacturing
plant in central Taiwan. The recruitment and selection of
study subjects have been described in detail previously (21).
Briefly, 790 male production line workers were recruited in
1998 and were invited to join again at the end of 2008. To
ensure study subjects without hypertension at baseline, we
excluded 10 workers because they reported having a physi-
cian diagnosis of hypertension and using antihypertensive
medication according to a questionnaire survey in 1998.
During the 10-year period, 86 workers retired and were lost
to follow-up. In addition, 116 subjects were rejected because
of the lack of follow-up results in 2008. Therefore, the study
group comprised 578 male production line workers. There
were no significant differences between the 578 participants
and the 202 nonparticipants at baseline in terms of employ-
ment duration, body mass index, high-density lipoprotein
level, triglyceride level, cigarette use, alcohol intake, and
regular exercise. The present study was reviewed and approved
by the Institutional Review Board of the School of Public
Health, China Medical University, before the study com-
menced in 2008, and written informed consent was obtained
again from each participant.
Blood pressure measurements and definition of
hypertension
The procedure for baseline blood pressure measurements
in 1998 was the same as that for the follow-up measurements
in 2008. All subjects were required to fast overnight before
blood sampling and blood pressure measurements during
annual health examinations. Subjects sat for 10 minutes in a
chair with back support before blood pressure was measured
bilaterally by a trained nurse using an automated sphygmo-
manometer (Ostar Model P2; Ostar Meditech Corp., Taipei,
Taiwan). The mean value of the 2 measurements was recorded
to represent the individual’s blood pressure in the present
study. Subjects were defined as hypertensive if they reported
a diagnosis of hypertension given by physicians after 1998,
if the mean value of their resting systolic blood pressure
(SBP) was ≥140 mm Hg in 2008, or if the mean value of
their resting diastolic blood pressure (DBP) was ≥90 mm Hg
in 2008. Height, body weight, total cholesterol level, and tri-
glyceride level were also measured in all subjects at baseline
and follow-up. The body mass index was calculated as
weight (kg)/height (m)2.
In addition, a self-administered questionnaire was used
to collect potential confounders in 1998 and 2008. These
Am J Epidemiol. 2013;177(8):818–825
Occupational Noise and Hypertension 819
factors included age, educational level, employment dura-
tion, cigarette use, alcohol intake, regular exercise, the use
of antihypertensive medication, and the use of hearing-
protective devices. Additional information (such as salt
intake and a family history of hypertension) was included
only in 2008. To avoid information bias, we defined the
lifestyle habits for regular users specifically (21, 34). The
use of hearing-protective devices included the percentage of
time that the subjects wore hearing-protective devices (i.e.,
never use, <2 hours’, 2–4 hours’, >4–6 hours’, and >6–8
hours’ working time) and the type of hearing-protective
devices (i.e., earplugs, earmuffs, or both). High salt-intake
workers were defined as those who reported ingesting food
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cooked with soybean sauce for more than one meal per day.
A subject was defined as having a family history of hyper-
tension if a positive answer was given to the question:
“Have your parents or grandparents been diagnosed with
hypertension by a physician in the past?” (21, 34).
Follow-up
We used employment personnel records to obtain each
subject’s first date of employment at this company and
assigned this date as the beginning of the follow-up period.
The end of the follow-up period was defined as either the
date of diagnosis by a physician or the date when the sub-
jects who had not been diagnosed with hypertension by a
physician were given their blood pressure examinations in
December 2008. Among the 141 cases classified as hyper-
tensive in this study, 56 cases were diagnosed with hyper-
tension (30 cases were taking antihypertensive medication),
and 85 cases were identified at the annual examination in
2008.
Noise exposure assessment
The procedure for noise exposure assessment in 1998
was similar to that for the follow-up measurements in
2008. We first identified 18 departments in this company
and divided each department into different locations on the
basis of the manufacturing processes by industrial hygien-
ists and senior workers. After the walk-through survey, we
measured the 15-minute time-weighted average equivalent
sound level by using a sound analyzer (Model TES-1358;
TES Electronic Corp., Taipei, Taiwan), which was calibrat-
ed with a sound-level calibrator (Model TES-1356; TES
Electronic Corp.) before environmental monitoring. The
short-term environmental sampling was performed at 337
locations that were possibly the loudest workplaces at this
company. For the 121 sites exhibiting a 15-minute time-
weighted average equivalent sound level of ≥65 A-weighted
decibels (dBA), additional 8-hour time-weighted average
measurements were conducted during September–December
of 1998. All subjects were divided into one of similar expo-
sure groups on the basis of the similarity and frequency
of tasks performed, the agents and processes with which
they worked, and the ways in which they performed the
tasks (35). Each subject was assigned a specific value of
noise exposure on the basis of the 8-hour time-weighted
average equivalent sound level measured in his workplace.
820 Chang et al.

Table 1. Baseline Characteristics of Study Participants, Taichung, Taiwan, 1998–2008

Exposure Groups
Total Subjects (n = 578)
Characteristics High (n = 152) Intermediate (n = 221) Low (n = 205) P Value
Mean (SD) No. % Mean (SD) No. % Mean (SD) No. % Mean (SD) No. %

Age at entry, 27.6 (4.6) 27.5 (5.4) 28.0 (5.6) 27.7 (5.3) 0.504a
years
Employment 10.2 (5.0)b 9.0 (4.8)c 10.9 (6.0) 9.8 (5.2) 0.003a
duration,
years
Body mass 24.0 (3.0) 23.8 (3.1) 23.6 (2.9) 23.8 (3.0) 0.493a
indexd
HDL, mg/dl 45.4 (6.9) 46.3 (10.6) 46.0 (8.3) 46.0 (8.9) 0.909a
LDL, mg/dl 115.1 (30.4) 114.5 (30.3) 112.3 (28.8) 113.8 (29.8) 0.609a

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Triglyceride, 142.2 (63.4) 143.6 (86.0) 156.7 (95.1) 147.7 (83.9) 0.347a
mg/dl
Education 63 41.5e 106 48.0e 50 24.4 219 37.9 <0.001f
(≤12
years)
Current 88 57.9 120 54.3 111 54.2 319 55.2 0.737f
smoking
(yes)
Alcohol 95 62.5 136 61.5 124 60.5 355 61.4 0.927f
drinking
(yes)
Regular 50 32.9 71 32.1 58 28.3 179 31.0 0.580f
exercise
(yes)
Use of hearing- <0.001f
protective
devices at
work
Never 39 25.7e,g 16 7.2e 121 59.0 176 30.4
<2 hours’ 80 52.6 35 15.8 26 12.7 141 24.4
working
time
2–4 hours’ 31 20.4 39 17.7 24 11.7 94 16.3
working
time
>4–6 1 0.7 59 26.7 10 4.9 70 12.1
hours’
working
time
>6–8 1 0.7 72 32.6 24 11.7 97 16.8
hours’
working
time

Abbreviations: HDL, high-density lipoprotein; LDL, low-density lipoprotein; SD, standard deviation.
a
Kruskal-Wallis test of the difference among the 3 groups.
b
Mann-Whitney test for a significant difference (P < 0.05) compared with the intermediate-exposure group.
c
Mann-Whitney test for a significant difference (P < 0.05) compared with the low-exposure group.
d
Body mass index: weight (kg)/height (m)2.
χ test for a significant difference (P < 0.05) compared with the low-exposure group.
e 2

χ test for the difference among the 3 groups.

f 2

χ test for a significant difference (P < 0.05) compared with the intermediate-exposure group.
g 2

To avoid an exposure bias due to the use of hearing-
protective devices at work, we calculated each participant’s
level of noise reduction according to the noise reduction
rating of the hearing-protective devices that he wore (29 dB
for earplugs and 25 dB for earmuffs), the protection levels
of the hearing-protective devices (an average of 28% for
earplugs and an average of 62% for earmuffs), a comfort
factor of 0.5 (because of the minimal percentage of comfort
related to compliance with usage of hearing-protective
devices) (36), and the percentage of working time that he
used the hearing-protective devices (36, 37). We used the
hearing-protective device-adjusted value of the 8-hour

Am J Epidemiol. 2013;177(8):818–825
 Occupational Noise and Hypertension 821

Table 2. Occupational Noise Exposure at Baseline in 3 Study Groups, Taichung, Taiwan, 1998–2008

Noise Levels (dBA) Before Noise Levels (dBA) After

Exposure Adjustment for Hearing Adjustment for Hearing
Groups Protective Devices Protective Devices
Mean (SD) Range Mean (SD) Range

High 87.4 (2.1)a,b 86.4–92.5 86.9 (2.2)a,b 85.3–92.5

Intermediate 85.4 (1.5)a 81.5–86.4 83.0 (1.3)a 80.3–84.8
Low 73.2 (9.4) 55.3–86.4 71.9 (9.0) 53.0–79.9
P value <0.001c <0.001c

Abbreviations: dBA, A-weighted decibel(s); SD, standard deviation.

a
Mann–Whitney test for a significant difference (P < 0.05) compared with the low-exposure group.
b
Mann–Whitney test for a significant difference (P < 0.05) compared with the intermediate-exposure group.

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c
Kruskal–Wallis test of the difference among the 3 groups.

time-weighted average equivalent sound level to classify
participants into 3 exposure groups by selecting the median
and third quartile as cutoff points in the distribution of
noise exposure among all subjects. The 578 workers were
subdivided into a high-exposure group (n = 152; noise
level: ≥85 dBA), an intermediate-exposure group (n = 221;
noise level: 80–<85 dBA), and a low-exposure group
(n = 205; noise level: <80 dBA).
Statistical analysis
We first used the Shapiro-Wilk test to determine the nor-
mality of continuous variables. The Kruskal-Wallis test was
then used to perform multiple comparisons of continuous
variables among the 3 groups for the nonnormal distribution,
and a 1-way analysis of variance was used for the same com-
parison of continuous variables that were normally distribu-
ted. We also used the χ2 test to compare the difference in
dichotomous variables among the 3 groups. For those
groups with significant differences, the Mann-Whitney test
(or t test) and the χ2 test were used to compare the high- and
intermediate-exposure groups with the low-exposure group
for continuous and dichotomous variables.
To compare individual differences in SBP and DBP
between the baseline and follow-up measurements, we used
the linear mixed-effect regression models for each exposure
group (38, 39). The fixed effects in the mixed model
included all variables in the final model at baseline and the
use of antihypertension medication in 2008. Individual sub-
jects were used as a random effect. We used the first-order
autoregressive model for covariance structures because of
the minimizing value of Akaike’s Information Criterion in
both SBP and DBP measurements (38, 39).
To avoid the information bias in observed person-years
due to the availability of only 1 blood pressure measurement
within the past 10 years, we identified hypertensive cases
by questionnaire, blood pressure measurements, and total
hypertensive cases used as the outcomes to perform the regres-
sion analyses. We used Cox proportional hazard regressions
and calculated relative risks with 95% confidence intervals
to compare the differences in incidence of hypertension
among groups while controlling for potential confounders.
We used a manual stepwise regression to build the final
model because only one variable of body mass index
(P = 0.005) was retained in the final step using an automatic
stepwise procedure. A basic model was examined first that
included age at baseline for biological plausibility and 2
dummy variables of exposure categories. The basic model
was then enlarged to include 2 variables (i.e., body mass
index and employment duration) that were significantly
associated with the risk of hypertension in the simple Cox
regression models. The final model included all variables in
the extended model and important risk factors of hyperten-
sion reported in the previous literature (32–33, 40), includ-
ing socioeconomic status (using educational levels or job
positions as surrogates), cigarette use, alcohol intake, and
regular exercise. In the sensitivity analysis, the 2 variables
of salt intake and family history of hypertension that had
been collected only in 2008 were included in the model.
The SAS standard package for Windows, version 9.2 (SAS
Institute, Inc., Cary, North Carolina), was used for the sta-
tistical analyses. The significance level was set at 0.050 for
all tests.
RESULTS
Table 1 summarizes the demographic characteristics of
578 participants at baseline. Significant differences were
identified among the exposure groups in the mean value of
employment duration, the number of individuals with an
educational level of ≤12 years, and whether individuals
used hearing-protective devices at work. Workers in the
high- and intermediate-exposure groups were more likely to
have an educational level of ≤12 years and were less likely
to never use hearing-protective devices at work than those
in the low-exposure group. In addition, high-exposure
workers had a significantly higher mean of employment
duration and were less likely to never use hearing-protective
devices at work compared with the intermediate-exposure
workers. In contrast, intermediate-exposure workers had a
significantly lower mean of employment duration than did
the low-exposure workers.
Table 2 shows the measurements of occupational noise
exposure for the 3 groups. Significant differences were

Am J Epidemiol. 2013;177(8):818–825
822 Chang et al.

Linear mixed-effect regression models were used to test the difference between the baseline and follow-up measurements after controlling for age at baseline, antihypertension
identified in the mean noise levels among the 3 groups

P Value

0.479b
either before or after an adjustment for hearing-protective
device use. The high- and intermediate-exposure groups

Baseline–Follow-up
were exposed to significantly higher mean values of noise

Differencea

−0.6, 3.2
−0.3, 3.2
0.1, 4.8
compared with the low-exposure group both before and

95% CI
after an adjustment for hearing-protective device use.
Table 3 shows the changes in blood pressure between
the baseline and follow-up measurements in the 3 groups. Al-
Mean

1.3
though there were no significant differences in SBP and DBP
1.4
2.5
among these 3 groups at baseline or follow-up, the SBP of
both the high-exposure (P = 0.035) and the intermediate-
P Value

0.194b
DBP, mm Hg

exposure (P < 0.001) groups significantly increased between

the baseline and follow-up measurements in the linear
Follow-up

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mixed-effect models. In addition, the DBP of high-exposure
Mean (SD)

81.6 (8.7)
82.5 (8.8)
83.3 (8.6)

workers significantly increased between the baseline and

follow-up measurements (P = 0.042) after controlling for po-
tential confounders.
The associations among the different groups and the risk
P Value

0.260b

of hypertension are summarized in Table 4. The multiple

Cox proportional hazard regression models showed that
Abbreviations: CI, confidence interval; DBP, diastolic blood pressure; SBP, systolic blood pressure; SD, standard deviation.
Baseline

workers exposed to 86.9 (standard deviation (SD), 2.2)

dBA and those exposed to 83.0 (SD, 1.3) dBA had a 1.93-
80.3 (11.2)
81.1 (10.8)
80.8 (12.9)

medication, body mass index, employment duration, educational level, cigarette use, alcohol intake, and regular exercise.
Mean (SD)

fold and a 1.75-fold relative risk of hypertension, respec-

tively, compared with those exposed to 71.9 (SD, 9.0) dBA
after an adjustment for potential confounders. There was a
significant dose-response relationship between the levels of
P Value

0.874b

noise exposure experienced by the 3 groups and the risk of

hypertension using total cases as the outcomes (adjusted
Baseline–Follow-up

relative risk (RR) = 1.35, 95% confidence interval (CI):

Differencea

−1.0, 4.0
2.5, 7.3
0.2, 6.2

1.06, 1.73). Similar results were found while using job

95% CI

positions (managers, engineers, administrators, and techni-

cians) instead of educational levels in the models. In addi-
tion, the intermediate-exposure group had a significantly
Table 3. Changes in Blood Pressure by Study Group, Taichung, Taiwan, 1998–2008

Mean

higher risk of measured hypertension than did the low-

1.5
4.9
3.2

exposure group.
In sensitivity analyses, the association between occupa-
P Value

One-way analysis of variance test of the difference among the 3 groups.

0.732b

tional noise exposure and the risk of hypertension persisted

SBP, mm Hg

for both the high-exposure (adjusted RR = 1.95, 95% CI:

Follow-up

1.16, 3.28) and the intermediate-exposure (adjusted

124.6 (13.9)
126.8 (14.4)
126.1 (15.3)
Mean (SD)

RR = 1.74, 95% CI: 1.08, 2.80) groups after the addition of

the 2 variables of salt intake and family history of hyperten-
sion to model 3. Furthermore, an increasing exposure-
response trend was found (adjusted RR = 1.37, 95% CI:
1.07, 1.75) (P = 0.014) in this sensitivity analysis. No signifi-
P Value

0.597b

cant differences were found among the 3 exposure groups

with regard to salt intake (P = 0.173) or family history of
Baseline

hypertension (P = 0.656).
123.1 (12.1)
122.0 (11.7)
122.9 (11.8)
Mean (SD)

DISCUSSION

We found a positive relationship between occupational noise

exposure ≥85 dBA at baseline and the 10-year incidence of
Person-

hypertension. The findings were consistent with the results in

2,873
3,020
1,912
Years

a retrospective study that reported a significantly higher risk

of hypertension in sawmill workers exposed to ≥85 dBA for
more than 30 years (10). Although their findings were
Intermediate
Exposure

limited to a misclassification of noise exposure because of no

Groups

adjustment for the use of hearing-protective devices at work,

High
Low

the 2 longitudinal studies reached similar results to show an

a

increased risk of hypertension following long-term chronic

Am J Epidemiol. 2013;177(8):818–825
 Occupational Noise and Hypertension 823

Table 4. Associations Between Different Noise Exposure Levels and Incidence of Hypertension, Taichung, Taiwan, 1998–2008

Outcomes by Different Noise No. of Crude RR Model 1a Model 2b Model 3c

Incidence
Exposure Levels, dBA Cases RR 95% CI ARR 95% CI ARR 95% CI ARR 95% CI
d
Diagnosed hypertension
<80 18 6.3 × 10−3 1 Referent 1 Referent 1 Referent 1 Referent
−3
80–<85 19 6.3 × 10 1.00 0.52, 1.90 1.00 0.53, 1.91 1.26 0.59, 2.70 1.16 0.54, 2.48
≥85 19 9.9 × 10−3 1.64 0.86, 3.12 1.65 0.87, 3.15 2.07 0.96, 4.45 2.05 0.96, 4.40
Ptrend 0.149 0.141 0.051 0.051
Measured hypertensione
<80 26 9.0 × 10−3 1 1 1 1
−3
80–<85 40 13.2 × 10 1.48 0.90, 2.42 1.49 0.90, 2.43 2.24 1.24, 4.05 2.22 1.20, 4.08

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≥85 19 9.9 × 10−3 1.19 0.66, 2.15 1.20 0.66, 2.16 1.82 0.92, 3.62 1.78 0.88, 3.59
Ptrend 0.452 0.438 0.101 0.136
Total hypertension
<80 44 15.3 × 10−3 1 Referent 1 Referent 1 Referent 1 Referent
80–<85 59 19.5 × 10−3 1.28 0.87, 1.89 1.28 0.87, 1.90 1.81 1.14, 2.89 1.75 1.09, 2.81
≥85 38 19.9 × 10−3 1.38 0.89, 2.13 1.39 0.90, 2.15 1.96 1.18, 3.27 1.93 1.15, 3.22
Ptrend 0.134 0.125 0.012 0.016

Abbreviations: ARR, adjusted relative risk; CI, confidence interval; dBA, A-weighted decibel(s); RR, relative risk.
a
The Cox proportional hazards regression adjusted for biological plausibility (i.e., age at baseline) as the basic model.
b
The Cox proportional hazards regression adjusted for age at baseline and significant factors in simple Cox regression models (such as
body mass index and employment duration) as the extended model.
c
The Cox proportional hazards regression adjusted for all variables in model 1, model 2, and important risk factors reported in previous
literature (i.e., educational level, cigarette use, alcohol intake, and regular exercise) as the final model.
d
Subjects reported that a physician had previously given them a diagnosis of hypertension.
e
Subjects had a mean value of resting systolic blood pressure of ≥140 mm Hg or a mean value of resting diastolic blood pressure of
≥90 mm Hg.

occupational noise exposure. Moreover, the present study
overcame the lack of individual risk factors of hypertension
in the previous study (10) to provide strong evidence that
hypertension was associated with occupational noise expo-
sure. We suggest that the currently regulated threshold for oc-
cupational noise exposure may expand the prevention of
noise-induced hearing loss (41) to the risk of hypertension,
which is a leading cause of cardiovascular diseases.
We also observed an exposure-response pattern between
noise-exposure levels and the risk of hypertension. Our
results were concordant with the findings in a cross-sectional
study showing that increasing noise exposure from 75 to
104 dBA was associated with an increasing prevalence of
hypertension in female textile mill workers (16). One
cohort study reported a significantly increasing risk of
hypertension with cumulative noise exposure ranging from
95 dBA × years to >115 dBA × years among male workers
(10). The same exposure metrics (i.e., 4 categories from
<85 dBA × years to ≥95 dBA × years) were applied to our
analyses, but no significant dose-response relationship
(adjusted RR = 1.03, 95% CI: 0.87, 1.21) was found in the
Poisson regression. The possible reason for different expo-
sure conditions resulting in the same dose-response associ-
ation might be that workers did not change jobs and tasks
in present and previous studies (16) and that there was turn-
over in another cohort (10).
In addition, the inverse-U–shaped dose-response rela-
tionship for measured hypertension indicated a role of
exposure duration in the etiology of the disease. Although
we used Cox regressions to account for varying time of ex-
posure, the magnitudes of effects on measured hyperten-
sion and diagnosed hypertension in the high-exposure
group were similar (i.e., around 2-fold), yet the effect
halved from 2.22 to 1.16 in the intermediate-exposure
group. These findings may indicate a “plateau” effect of ex-
posure intensity that is independent of exposure duration.
Therefore, when the exposure intensity is not the highest,
the exposure duration is likely the second component of ex-
posure that “kicks in” the dysregulation of the nervous and
hormonal systems, leading to the disease.
The significant increases in SBP between the baseline
and follow-up measurements were also observed among
workers exposed to 80–<85 dBA and those exposed
to ≥85 dBA. These findings were consistent with the
results in a cohort study showing that male workers
exposed to ≥85 dBA and using hearing-protective devices
had a mean increase of 3.8 mm Hg in SBP over 9 years of
follow-up, which is a significantly higher increase than that
observed in office workers (11). Additionally, workers
exposed to ≥85 dBA exhibited a significant increase in
DBP between the baseline and follow-up measurements as
well as a significantly higher DBP at follow-up compared

Am J Epidemiol. 2013;177(8):818–825
824 Chang et al.
with those exposed to <80 dBA. These findings provided
the evidence to explain the association between occupation-
al noise exposure above 85 dBA and the higher risk of
hypertension.
The strengths of the present study include a cohort-study
design, detailed assessments of personal exposure histories,
and comprehensive controls for most potential confounders
of hypertension. In addition, occupational noise exposure
adjusted for the use of hearing-protective devices may
avoid the misclassification of study subjects and an over-
estimation of noise exposure to produce the consistent results
associated with road traffic noise exposure in environmental
epidemiologic studies (34, 42).
Testing for the validity of noise exposure assessment was
also conducted to check the precision and accuracy of a
predictive model, and noise levels accounted for the use of
hearing-protective devices. Although information from
departments, processes, job positions, and noise measure-
ments collected in 1998 was used to establish a predictive
model of noise levels, the adjusted R 2 was 0.93 in a multi-
ple linear regression. In a comparison of environmental
measurements at 11 locations in 2004, the bias and preci-
sion in this model were 2.4 (SD, 4.9) dBA to produce an
accuracy of 5.5 dBA, which showed an overestimation due
to engineering controls over time. In contrast, the bias and
precision of 2-stage noise measurements accounting for the
use of hearing-protective devices among study subjects
were 1.5 (SD, 2.0) dBA to have an accuracy of 2.5 dBA.
Such comparisons indicated that assessment of exposure by
using the worst-case scenario might be inaccurate while
still being precise.
One limitation of this study is the overestimation of indi-
vidual cumulative levels in occupational noise exposure.
Noise levels measured 10 years ago have obviously been
reduced in response to the requirement for the improvement
of engineering controls in the workplace. Therefore,
workers assigned to the high-exposure group in 1998 might
be exposed to <85 dBA in 2008. A comparison of environ-
mental noise levels between the baseline and follow-up in
all subjects showed that the mean value of noise levels
measured in 2008 (77.6 (SD, 7.6) dBA) was significantly
lower than that measured in 1998 (81.6 (SD, 8.5) dBA)
( paired t test, P < 0.001). The overall decrease of 5.2 (SD,
9.3) dBA had apparent decreases in the processes of
peripheral element assembly (−9.7 (SD, 16.4) dBA) and
forging and casting (−7.3 (SD, 7.7) dBA) that might
reduce the proportion of the use of hearing-protective
devices from 73.3% to 27.7% and from 85.7% to 61.9%,
respectively. Because no subjects changed their jobs or
tasks, the systematic overestimation of cumulative noise
exposure was equally distributed across different groups,
and the nondifferential misclassification of exposure might
attenuate the estimates toward the null. However, our find-
ings still observed the significant relationship between
occupational noise exposure and the risk of hypertension.
The other limitation is that noise exposure, blood pres-
sure, and other important risk factors of hypertension were
not measured continuously over the past 10 years. The sig-
nificantly higher risk of hypertension among the workers
exposed to ≥85 dBA might be because they experienced
the greatest changes in lifestyle. However, this reason
seems improbable because the prevalence rates of risk
factors related to hypertension, such as cigarette use (58%)
and alcohol intake (63%), declined significantly (27% and
21%, respectively; both P’s < 0.001) in the high-exposure
group at the follow-up examination. In addition, blood
pressure was measured twice over the past 10 years. This is
our first attempt to longitudinally observe the occupational
noise exposure and the incidence of hypertension among
these workers. The 4-year period of follow-up will continue
in 2012 to circumvent limitations imposed by lifestyle
changes over time and to have additional measurements of
noise exposure and blood pressure.
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In summary, the present study showed that occupational
exposure to noise levels of ≥85 dBA was associated with
the development of hypertension and that there was a dose-
response relationship between noise exposure and the 10-
year incidence of hypertension. The association between
occupational noise exposure of ≥85 dBA and the risk of
hypertension might be due to the increases of SBP and
DBP observed in the present study. The currently regulated
threshold for occupational noise exposure may prevent the
adverse health effects from noise-induced hearing loss to
the development of hypertension.
ACKNOWLEDGMENTS
Author affiliations: Department of Occupational Safety
and Health, College of Public Health, China Medical Uni-
versity, Taichung, Taiwan, Republic of China (Ta-Yuan
Chang, Bing-Fang Hwang, Ren-Yin Chen, Ven-Shing
Wang, Jim-Shoung Lai); Institute for Risk Assessment Sci-
ences, Utrecht University, Utrecht, the Netherlands
(Ta-Yuan Chang); Department of Family Medicine, China
Medical University Hospital, Taichung, Taiwan, Republic
of China (Chiu-Shong Liu); School of Medicine, College
of Medicine, China Medical University, Taichung, Taiwan,
Republic of China (Chiu-Shong Liu); and Department of
Pharmacy, College of Pharmacy, China Medical University,
Taichung, Taiwan, Republic of China (Bo-Ying Bao).
This study was supported by grant NSC 97-2221-E-039-
007-MY3 from the National Science Council, Taiwan.
We thank the National Science Council, Taiwan, for
financial support. We thank Deng-Tsai Lai for his contribu-
tions to this study. We also thank the graduate students who
assisted with environmental sampling at the workplace.
Conflict of interest: none declared.
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